Sports Injuries of the Hand and Wrist [1st ed.] 978-3-030-02133-7, 978-3-030-02134-4

Table of contents :
Front Matter ....Pages i-xv
Mallet Finger Injuries (Loris Pegoli, Giorgio Pivato)....Pages 1-13
Flexor Digitorum Profundus Avulsion Injuries (Heather L. Baltzer, Steven L. Moran)....Pages 15-34
Fractures and Dislocations of the Proximal Interphalangeal Joint (David J. Shewring)....Pages 35-58
Phalangeal Fractures in the Athlete (James Logan, David Warwick)....Pages 59-79
Climber’s Pulley Injuries (François Moutet, M. Bouyer, Denis Corcella, Alexandra Forli, Alessandro Semere)....Pages 81-99
Metacarpal Fractures in the Athletes (Alistair R. Phillips, David G. Hargreaves)....Pages 101-123
Thumb Fractures (Mohamed Noureldin, Sanjeev Kakar)....Pages 125-150
Hand Injuries in the Elite Boxer (Mike Hayton, David Dickson)....Pages 151-159
Scaphoid Fractures (Joel V. Ferreira, Juan Marcelo Giugale, Mark Baratz)....Pages 161-183
Carpal Fractures (Excluding Scaphoid) (Carlos Heras-Palou)....Pages 185-200
Scapholunate Ligament Injury (Jonathan Adamthwaite, Sina Babazadeh, Marc Garcia-Elias)....Pages 201-234
Injuries to the Triangular Fibrocartilage Complex (Mark Rekant)....Pages 235-253
Injuries to the Extensor Carpi Ulnaris and Its Investments in the Athlete (Rodney J. French, Thomas J. Graham)....Pages 255-276
Chronic Exertional Compartment Syndrome (CECS) of the Forearm (John W. K. Harrison)....Pages 277-288
Back Matter ....Pages 289-295

Citation preview

In Clinical Practice

Mike Hayton · Chye Yew Ng · Lennard Funk Adam Watts · Mike Walton Editors

Sports Injuries of the Hand and Wrist

In Clinical Practice

Taking a practical approach to clinical medicine, this series of smaller reference books is designed for the trainee physician, primary care physician, nurse practitioner and other general medical professionals to understand each topic covered. The coverage is comprehensive but concise and is designed to act as a primary reference tool for subjects across the field of medicine. More information about this series at http://www.springer. com/series/13483

Mike Hayton  •  Chye Yew Ng Lennard Funk  •  Adam Watts Mike Walton Editors

Sports Injuries of the Hand and Wrist

Editors

Mike Hayton Upper Limb Unit Wrightington Hospital Wigan, UK

Chye Yew Ng Upper Limb Unit Wrightington Hospital Wigan, UK

Lennard Funk Upper Limb Unit Wrightington Hospital Wigan, UK

Adam Watts Upper Limb Unit Wrightington Hospital Wigan, UK

Mike Walton Upper Limb Unit Wrightington Hospital Wigan, UK

ISSN 2199-6652     ISSN 2199-6660 (electronic) In Clinical Practice ISBN 978-3-030-02133-7    ISBN 978-3-030-02134-4 (eBook) https://doi.org/10.1007/978-3-030-02134-4 Library of Congress Control Number: 2019930724 © Springer Nature Switzerland AG 2019 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

Foreword

Injuries to athletes can be devastating, often negating the hours or even years of training. Over the years, sports performance has become a specialty in its own right, and the management of injuries generated both in and out of the sports environment has improved immensely. Improvements in investigation and improvements in understanding of the mechanism of injury and understanding the most efficacious use of surgery and therapy have improved the quality of life of innumerable injured sports persons. The editors have brought together a stellar constellation of experts, all of whom bring to the book their own special expertise and understanding of their area of expertise. There is no doubt that the information, which the ­collective body has produced, will make a significant difference to the recognition and treatment of sports injuries in the upper limb. Wrightington, UK

John K. Stanley

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Preface

This book serves as an introduction to the management of common sports injuries of the hand and wrist. We hope this will be of use to students, therapists, physicians and surgeons who are interested in understanding the pathoanatomy and latest treatment options for these injuries. We are particularly grateful to the authors for their valuable contributions to the book. Wigan, UK Wigan, UK

ChyeYew Ng Mike Hayton

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Acknowledgment

We are grateful to our families (Philippa and Shi Zhuan), friends and colleagues for their patience during this project.

ix

Contents

1 Mallet Finger Injuries ���������������������������������������������������   1 Loris Pegoli and Giorgio Pivato 2 Flexor Digitorum Profundus Avulsion Injuries ���������  15 Heather L. Baltzer and Steven L. Moran 3 Fractures and Dislocations of the Proximal Interphalangeal Joint�����������������������������������������������������  35 David J. Shewring 4 Phalangeal Fractures in the Athlete�����������������������������  59 James Logan and David Warwick 5 Climber’s Pulley Injuries�����������������������������������������������  81 François Moutet, M. Bouyer, Denis Corcella, Alexandra Forli, and Alessandro Semere 6 Metacarpal Fractures in the Athletes���������������������������101 Alistair R. Phillips and David G. Hargreaves 7 Thumb Fractures������������������������������������������������������������� 125 Mohamed Noureldin and Sanjeev Kakar 8 Hand Injuries in the Elite Boxer ��������������������������������� 151 Mike Hayton and David Dickson 9 Scaphoid Fractures��������������������������������������������������������� 161 Joel V. Ferreira, Juan Marcelo Giugale, and Mark Baratz

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Contents

10 Carpal Fractures (Excluding Scaphoid)����������������������� 185 Carlos Heras-Palou 11 Scapholunate Ligament Injury�������������������������������������201 Jonathan Adamthwaite, Sina Babazadeh, and Marc Garcia-Elias 12 Injuries to the Triangular Fibrocartilage Complex��������������������������������������������������������������������������� 235 Mark Rekant 13 Injuries to the Extensor Carpi Ulnaris and Its Investments in the Athlete ������������������������������������������� 255 Rodney J. French and Thomas J. Graham 14 Chronic Exertional Compartment Syndrome (CECS) of the Forearm������������������������������������������������� 277 John W. K. Harrison Index����������������������������������������������������������������������������������������� 289

Editors

Mike  Hayton  Upper Limb Unit, Wrightington Hospital, Wigan, UK Chye  Yew  Ng  Upper Limb Unit, Wrightington Hospital, Wigan, UK

Contributors Jonathan Adamthwaite  Department of Plastic Surgery, York Teaching Hospital NHS Foundation Trust, York, UK Sina Babazadeh  Institut Kaplan, Barcelona, Spain Heather  L.  Baltzer  Division of Plastic Surgery and Orthopedic Surgery, Toronto Western Hospital, Toronto, ON, Canada Mark  Baratz  Hand and Upper Extremity, Department of Orthopaedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, PA, USA M. Bouyer  Clinique de Chirurgie Réparatrice de la Main et des Brûlés SOS Main Grenoble, CHU de Grenoble Hôpital A. Michalon, Grenoble, France Denis  Corcella  Clinique de Chirurgie Réparatrice de la Main et des Brûlés SOS Main Grenoble, CHU de Grenoble Hôpital A. Michalon, Grenoble, France xiii

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Editors

David  Dickson  Department of Orthopaedics, Bradford Royal Infirmary, Bradford, UK Joel V. Ferreira  Department of Orthopaedic Surgery, UConn Health, Farmington, CT, USA Alexandra  Forli  Clinique de Chirurgie Réparatrice de la Main et des Brûlés SOS Main Grenoble, CHU de Grenoble Hôpital A. Michalon, Grenoble, France Rodney J. French  Surgery of the Hand and Wrist, Division of Plastic Surgery, University of British Columbia, Vancouver, BC, Canada Marc Garcia-Elias  Institut Kaplan, Barcelona, Spain Juan  Marcelo  Giugale  Greater Pittsburgh Orthopaedic Associates, Pittsburgh, PA, USA Thomas  J.  Graham  Department of Orthopedic Surgery, NYU Langone Health, New York, NY, USA David  G.  Hargreaves  Department of Orthopaedics, University Hospital Southampton NHS Foundation Trust, Southampton, UK John  W.  K.  Harrison  Department of Orthopaedics, Gateshead NHS Foundation Trust, Gateshead, UK Carlos  Heras-Palou  Pulvertaft Hand Centre, Royal Derby Hospital, Derby, UK Sanjeev  Kakar  Department of Orthopedic Surgery, Mayo Clinic, Rochester, MN, USA James Logan  Department of Orthopaedics, University Hospitals Southampton NHS Foundation Trust, Southampton, UK Steven L. Moran  Department of Orthopaedic Surgery, Mayo Clinic, Rochester, MN, USA François  Moutet  Clinique de Chirurgie Réparatrice de la Main et des Brûlés SOS Main Grenoble, CHU de Grenoble Hôpital A. Michalon, Grenoble, France

Editors

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Mohamed  Noureldin  Department of Orthopedic Surgery, Mayo Clinic, Rochester, MN, USA Loris  Pegoli  Hand and Reconstructive Microsurgery Department, Humanitas University, Milan, Italy Alistair  R.  Phillips  Department of Orthopaedics, University Hospital Southampton NHS Foundation Trust, Southampton, UK Giorgio  Pivato  San Pio X Clinic, Hand and Reconstructive Microsurgery Unit, Milan, Italy Mark  Rekant  Philadelphia Hand to Shoulder Center, Department of Orthopaedic Surgery, Thomas Jefferson University, Philadelphia, PA, USA Alessandro Semere  Clinique de Chirurgie Réparatrice de la Main et des Brûlés SOS Main Grenoble, CHU de Grenoble Hôpital A. Michalon, Grenoble, France David J. Shewring  Department of Trauma and Orthopaedic Surgery, University Hospital of Wales, Cardiff, UK David  Warwick  Department of Orthopaedics, University Hospital Southampton NHS Foundation Trust, Southampton, UK

Chapter 1 Mallet Finger Injuries Loris Pegoli and Giorgio Pivato

Key Learning Points • Mallet injury is often ignored by the athlete leading to delayed presentation that may compromise the final outcome. • The decision-making for treatment relates to the presence of a bony fragment and joint subluxation. • Complications of surgery include skin necrosis, recurrent extensor lag, nail deformities and infection.

Introduction Mallet finger is a common athletic injury, in which a loss of extension of the distal phalanx occurs. It has been described as the most common closed tendon injury in athletes [2], L. Pegoli (*) Hand and Reconstructive Microsurgery Department, Humanitas University, Milan, Italy e-mail: [email protected] G. Pivato Hand and Reconstructive Microsurgery Unit, San Pio X Clinic, Milan, Italy © Springer Nature Switzerland AG 2019 M. Hayton et al. (eds.), Sports Injuries of the Hand and Wrist, In Clinical Practice, https://doi.org/10.1007/978-3-030-02134-4_1

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with baseball, softball, basketball and volleyball being the most frequently involved sports [6, 12]. It may occur due to a tendinous lesion, which may be a stretch or a complete tear of the tendon, or due to a bony avulsion at the level of the extensor tendon’s insertion at the base of the distal phalanx. In all cases, the result is variable loss of the active extension of the distal phalanx [1]. It is usually caused by forced flexion of an extended finger such as when the tip of the finger is jammed against an object such as a ball or another player.

Clinical Setting Following a mallet injury, pain may not necessarily be significant initially. The only noticeable deformity is a droop at the distal interphalangeal joint (DIPJ) with loss of active extension (Fig.  1.1). This is eventually associated with tenderness and swelling at the dorsal aspect of the DIPJ.  Due to the seemingly minor nature of the injury, it is often ignored by the athlete leading to delayed presentation that may compromise the final outcome.

Figure 1.1  Typical droop at the DIPJ due to a mallet injury

Chapter 1.  Mallet Finger Injuries

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Figure 1.2  Swan-neck deformity

Diagnosis Proper understanding of the complex anatomy of the extensor tendons is crucial to making the correct diagnosis. If left untreated or poorly managed, there is a high risk of developing swan-neck deformity (Fig.  1.2), resulting in permanent functional impairment. The diagnosis is essentially clinical with the droop posture at the DIPJ associated with a variable loss of extension. Radiographs (AP and lateral views) centred at the DIPJ of the injured digit are obtained to exclude an avulsion fracture. Furthermore, one should evaluate the presence of joint subluxation on the true lateral view.

Classification The injury may be classified using Doyle’s classification, which considers the presence of a wound, the different involvement of tissues as well as the amount of the articular surface involved (Table 1.1).

Treatment In acute setting, the initial treatment is to immobilise the finger in neutral extension and cool the finger with an ice pack.

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Table 1.1  Doyle’s classification TYPE I Closed injury, with or without small dorsal avulsion fracture II Open injury: laceration III Open injury (deep abrasion involving skin and tendon substance) IV Fracture (Mallet fracture) IV A Distal phalanx physeal injury (paediatric) IV B Fracture fragment involving 20% to 50% of articular surface (adult) IV C Fracture fragment >50% of articular surface (adult)

The patient is then referred to a hand specialist for further assessment. The decision-making for treatment relates to the presence of a bony fragment and joint subluxation.

Conservative Pure Tendinous Lesion In the presence of a pure tendinous lesion with moderate loss of extension (up to 20°), conservative treatment is generally recommended. If conservative option is employed, we recommend a custom-­made splint to be applied for 6  weeks continuously (Fig. 1.3). The DIPJ should be splinted in slight hyperextension to re-approximate the extensor tendon and the distal phalanx. It is mandatory for the finger to remain fully extended at all times. While maintaining extension can be difficult, proper education could improve compliance. We prefer the splint to be positioned dorsally as to leave the pulp free. When applying the splint, full motion of the proximal interphalangeal joint should be permitted. Other authors have described the use of a skin-tight plaster with good results. Prefabricated plastic splints are readily available, but we have found them to be either too tight or too loose.

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Figure 1.3  A custom-made splint to keep the DIPJ in slight hyperextension

Weekly follow-ups are scheduled to check the proper position and to adjust the splint size. After this period if an improvement is seen, a further 2 weeks of night splinting is suggested together with a hand rehabilitation protocol to improve the range of motion of the DIPJ.

Surgical Pure Tendinous Lesion In cases with a severe degree of flexion deformity, which could imply greater disruption of the extensor insertion, some may consider primary surgical repair.

Acute Under digital or metacarpal block anaesthesia, an H-shaped incision is performed dorsally at the level of the DIPJ (Fig. 1.4). Dissection is carried out as far as the extensor tendon is isolated. During this dissection, beware not to traumatise the skin, which is extremely thin at this level. A 1.2 mm K-wire is

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Figure 1.4  H-shaped incision

then inserted across the DIPJ holding the distal phalanx in about 10° of hyperextension. Whenever it is possible to isolate the two ends of the tendon, an end-to-end suture repair is advised. We prefer to use a mattress suture due to the thinness of the tendon. If an end-to-end suture is not possible, a suture anchor or pullout repair may be performed. While suturing the skin, tenodermodesis could be performed to augment the repair. It consists of removing an ellipse of the dorsal skin and closing the wound together with underlying tissue (Fig. 1.5).

Chronic In chronic lesions (older than 2–3  months), it is extremely rare to find good-quality tendon tissue that would allow a direct repair. In cases where the flexion of the DIPJ is greater than 20° (especially if the index finger is involved), we would consider interphalangeal joint fusion.

Chapter 1.  Mallet Finger Injuries

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Figure 1.5  Tenodermodesis is performed by removing an ellipse of skin and closing the wound with underlying tissue

Mallet Fracture In the presence of a bony avulsion (Fig. 1.6), if less than 20% of the articular surface is involved, the injury may be treated as a tendinous lesion. If the fragment is larger, fixation may be considered. Many procedures have been proposed such as screw fixation, interosseous wiring, pullout wiring fixation and percutaneous pinning fixation [3, 4, 7–9, 11]. We favour extension block technique, as described by Ishiguro [3]. Main indications include acute injuries, presence of a large bony fragment, volar subluxation and loss of joint congruity. A fracture presenting later than 5 weeks is a relative indication for fixation. In such case, the fracture site may be freshened up by percutaneous debridement using a needle. Under digital block anaesthesia, both the distal and the proximal interphalangeal joints are held in maximum flexion (Fig.  1.7). Under the guidance of the image intensifier, a K-wire is inserted percutaneously through the terminal

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Figure 1.6  A bony mallet injury

Figure 1.7 The DIPJ is flexed maximally to reduce the avulsion fragment

extensor tendon, at 1–2 mm dorsal and proximal to the fracture fragment, into the middle phalanx. While performing this step, attention should be given to the preoperative X-ray. The fragment is not necessarily right

Chapter 1.  Mallet Finger Injuries

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Figure 1.8  A dorsal blocking K-wire in-situ

on the middle axis of the phalanx, so the wire needs to be inclined accordingly in order to block the fragment effectively (Fig. 1.8). The distal phalanx is then pulled distally and extended in order to reduce the fracture. The key is to maintain about 15° of flexion of the DIPJ so as to avoid diastasis of the two fragments. Next the DIPJ is immobilised with a second oblique percutaneous K-wire, which runs palmar to the fracture. Following satisfactory fixation, the extension block wire is bent palmarly, so as to apply a compression force to the fracture itself (Fig. 1.9).

Postoperative Treatment A splint (as described above) is then applied to maintain the DIPJ in 30–40° of flexion. Both wires are removed after 4–6 weeks or once there is radiological evidence of healing. The patient is educated to massage the dorsal scar.

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Figure 1.9  Extension blocking and axial K-wires inserted to hold the reduction

Complications Conservative Treatment Conservative treatment of mallet fingers is not without problems. Main complications include dorsal pressure on the DIPJ due to the splint causing skin necrosis [5] and persistent extensor lag.

Surgical Treatment Intraoperatively, fragmentation of the main fragment could occur. King et al. [5] reported that 41% of surgically treated mallet fractures developed postoperative complications such as marginal skin necrosis, recurrent extensor lags, permanent nail deformities (Fig. 1.10) and infections, which may adversely affect the outcome [10]. Other complications include delayed union, malunion and secondary osteoarthritis.

Chapter 1.  Mallet Finger Injuries

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Figure 1.10  An example of nail deformity

Summary Mallet finger is a common sports injury. Careful management with attention to details is crucial to achieving a satisfactory outcome. The initial treatment involves immobilising the DIPJ in neutral position, followed by X-ray examination to check for any fracture and joint subluxation. Regardless of the definitive treatment, which could be either conservative or surgical, careful follow-up is necessary to minimise the risk of complications.

Questions and Answers 1. Radiograph is not compulsory in the assessment of mallet injury? True or False. A: False. There could be associated bony avulsion and joint subluxation.

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2. What are the potential complications of surgery for mallet finger? A: Skin necrosis, recurrent extensor lag and nail deformity 3. What is the potential chronic deformity of neglected mallet injury? A: Swan-neck deformity

References 1. Brody GA. Tendon ruptures: mallet, FDP in football. Hand Clin. 2012;28(3):435. 2. Chauhan A, Jacobs B, Andoga A, Baratz ME. Extensor tendon injuries in athletes. Sports Med Arthrosc. 2014;22(1):45–55. 3. Ishiguro T.  A new method of closed reduction for mallet fractures. J Jpn Soc Surg Hand. 1988;1:444–7. 4. Jupiter JB, Sheppard JE. Tension wire fixation of avulsion fractures in the hand. Clin Orthop Relat Res. 1987;214:113–20. 5. King HJ, Shin SJ, Kang ES.  Complications of operative treatment for mallet fractures of the distal phalanx. J Hand Surg Br. 2001;26(1):28–31. 6. Ouellette EA. Tendon ruptures: mallet, FDP and ECRB tendon ruptures associated with lunotriquetral coalitions in professional basketball players. Hand Clin. 2012;28(3):433–4. 7. Pegoli L, Toh S, Arai K, Fukuda A, Nishikawa S, Vallejo IG. The Ishiguro extension block technique for the treatment of mallet finger fracture: indications and clinical results. J Hand Surg Br. 2003;28(1):15–7. 8. Sakaue M, Sumimoto Y, Omori K, Yoshida M.  Treatment of mallet finger using a microscrew. J Jpn Soc Surg Hand. 1986;3:538–41. 9. Scalcione LR, Pathria MN, Chung CB.  The athlete’s hand: ligament and tendon injury. Semin Musculoskelet Radiol. 2012;16(4):338–49. 10. Shimura H, Wakabayashi Y, Nimura A.  A novel closed reduction with extension block and flexion block using Kirschner wires and microscrew fixation for mallet fractures. J Orthop Sci. 2014;19(2):308–12.

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11. Shin SS.  Baseball commentary-tendon ruptures: mallet, FDP. Hand Clin. 2012;28(3):431–2. 12. Uslu M, Solak K, Ozsahin M, Uzun H.  Bilateral volleyball-­ related deformity of the little fingers: mallet finger and clinodactyly mimic. J Sports Sci Med. 2011;10(1):227–9.

Chapter 2 Flexor Digitorum Profundus Avulsion Injuries Heather L. Baltzer and Steven L. Moran

Key Learning Points 1. Describe the mechanism of flexor digitorum profundus injuries. 2. Review the pertinent anatomy and its application to the Leddy-Packer classification of these injuries. 3. Provide an overview of management based on Leddy-­Packer type of injury and timing of injury.

Etiology Closed flexor digitorum profundus (FDP) avulsion injuries are one of the more common forms of Zone I flexor tendon injuries. The mechanism of tendinous avulsions involves H. L. Baltzer Division of Plastic Surgery and Orthopedic Surgery, Toronto Western Hospital, Toronto, ON, Canada S. L. Moran (*) Department of Orthopaedic Surgery, Mayo Clinic, Rochester, MN, USA e-mail: [email protected] © Springer Nature Switzerland AG 2019 M. Hayton et al. (eds.), Sports Injuries of the Hand and Wrist, In Clinical Practice, https://doi.org/10.1007/978-3-030-02134-4_2

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forced hyperextension of a maximally flexed distal ­interphalangeal joint (DIPJ). These injuries often arise during tackling sports [1], while the fingers tightly grasp the jersey of the player being tackled, with subsequent forced extension of the finger when the player escapes the tackle. This common mechanism has led to the term “jersey finger” to label this particular type of injury; however, it can be seen in both athletes and nonathletes.

Relevant Anatomy The FDP muscle originates from the proximal two-thirds of the ulna and the interosseous membrane. The FDP tendons to the small, ring, and long finger often share a common muscle belly, while the index FDP tendon often has an independent muscle belly [2]. Before inserting into the volar base of the distal phalanx, the FDP tendons pass into the flexor tendon sheath with the flexor digitorum superficialis (FDS) tendons. The profundus tendon passes deep to the superficialis until the level of Camper’s chiasm where it passes through the FDS; it then travels superficial to the FDS insertion (Fig. 2.1). A system of small mesenteries exist within the flexor tendon sheath termed vincula that are a major source of blood supply for the distal flexor tendons (Fig. 2.1). Both the FDS and FDP tendons are each supplied by two vincula, termed the longus and the brevis. The vinculum profundus brevis (VPB) is present proximal to the insertion of FDP tendon at the distal metaphysis of the middle phalanx, and the vinculum profundus longus (VPL) arises from the FDS tendon at the level of the PIP joint. The VPB is disrupted with an FDP avulsion injury, and the VPL may be disrupted with a Type I injury (see below). The disruption of one or both vincula is an important consideration as disruption of the tendons’ blood supply can limit the capacity for tendon healing following repair [3, 4]. In addition, intact vincula can prevent the profundus tendon from retracting into the palm or forearm.

Chapter 2.  Flexor Digitorum Profundus Avulsion Injuries

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a

VBP VLP VBS

VLS

b

VBP VLP VBS VLS

Figure 2.1  Demonstration of the relationship of the FDP and FDS and their relative insertion points including the locations of the vincula longus and brevis for the profundus and superficialis tendons. (a) Artists rendition of the finger showing the position of the vincula. (VBP) vincula brevis profundus, (VLP) vincula longus profundus, (VBS) vincula brevis superficalis, (VLS) vincula longus superficialis. (b) shows vascular supply to tendons entering through vincula. ((a) Taken from J Am Acad Orthop Surg 2011;19: 152–162; (b) taken from Green’s Operative Hand Surgery, editor: Wolfe, chapter 7 page 193)

The distal portion of the FDP tendon has dual vascular supply, which includes both the vincular system and an interosseous supply originating from the distal phalanx [5]. These interosseous vessels from the distal phalanx enter the FDP tendon at its insertion and are disrupted with avulsion injuries.

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Rupture of the FDP most commonly occurs at its insertion point into the distal phalanx rather than the musculotendinous junction in the forearm. Intratendinous profundus ruptures are rare and are usually associated with a traumatic amputation of the distal phalanx or are secondary to attritional wear from mechanical irritation such as bone spurs, inflammatory tendinopathies, and tenosynovitis [6]. Although FDP avulsion injuries can affect any finger, they occur most often in the ring finger [7]. Purported explanations for this include a less robust insertion of the ring finger FDP tendon in the base of the distal phalanx [7] and the more prominent position of the tip of the ring finger during power grip [8]. The latter causes the ring finger to experience more force than other digits during pull-away testing.

Classification The tendinous avulsions can occur with or without a bony fragment from the base of the distal phalanx. The avulsed tendon then retracts proximally. The degree of retraction is dependent upon two factors: the first is the presence of a bony fragment attached to the distal end of the avulsed FDP tendon that limits retraction through the flexor tendon sheath; and the second is the maintenance of an intact VPL. The original classification of these injuries was developed by Leddy and Packer and is still used widely today. The Leddy-Packer system is a three-part classification (Types I–III) based on the level of retraction of the tendon and the presence of a bony fragment on radiographs [1]. Type I injuries represent avulsions of the tendon from the distal phalanx with disruption of both the longus and brevis vincula and resultant proximal tendon stump retraction into the palm. In a Type II injury, the avulsed tendon retracts to the level of the FDS decussation at the PIP joint where the VPL arises. The VPB is disrupted, while the long vinculum remains intact, tethering the ruptured tendon at the level of the PIP joint. A small bone fragment may be attached to the retracted tendon stump, aiding in the radiographic diagnosis. The tendon length is preserved relative to Type I injuries.

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Type II injuries have been reported to be the most common form of avulsion injury [9]. In Type III injuries, a large bony fragment from the distal phalanx remains with the profundus. The tendon stump and bony fragment typically cannot retract further than the level of the A4 pulley. Due to bone fragment, the tendon cannot retract, so both vincula remain intact with Type III injuries. Since the original description by Leddy and Packer, two additional injury types have been described [10–13]. Type IV injuries describe an avulsion injury in which a large cortical fragment of the base of the distal phalanx is held at the level of the A4 pulley with concomitant FDP avulsion off of this fragment. The tendon can either retract to the level of the PIP joint or into the palm. Type V injuries describe both a distal phalanx avulsion fracture with additional distal phalanx fractures [12]. A recent review on this topic found that Types I–III are more commonly reported injuries with Types IV and V being reported less frequently. Approximately 50% of FDP avulsion injuries are associated with a bony fragment [3].

Diagnosis of FDP Avulsion Injuries Clinical Physical examination will reveal a disruption of the cascade of the fingers at rest with the affected finger in a more extended position (Fig.  2.2). There may be swelling and ecchymosis of the affected digit. Palpation along the flexor tendon sheath may reveal an area of point tenderness, which may signify the location of the avulsed tendon stump [14]. The pathognomonic finding is loss of DIP joint flexion in the affected digit with attempts to make a fist. The diagnosis may be delayed as flexion is preserved at the metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints, secondary to the lumbricals and intact FDS tendons, respectively [14]. Pain and swelling may also complicate the physical exam and limit movement of the fingers. In this scenario, administration of local anesthetic to facilitate a thorough physical examination may be warranted in order to prevent a delay in appropriate referral and treatment.

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Imaging Specifying the level of tendon retraction is critical as it will dictate the surgical approach. Plain radiographs are indicated for all suspected FDP avulsion injuries for identifying distal phalanx fractures and avulsed bony fragments (Fig. 2.3). Soft tissue imaging modalities, including ultrasound and magnetic resonance imaging (MRI), can provide useful information to assist with localizing the level of retraction when findings on physical examination are equivocal [15]. Ultrasound is the more commonly used modality but has been shown to be operator dependent [16].

Treatment The factors influencing the prognosis include the proximal extent of tendon retraction, the presence and size of bony fragments, and the delay between injury and treatment [1, 17]. All FDP avulsion injuries should undergo prompt treatment to prevent more proximal migration of the tendon and contraction of the musculotendinous unit. Injuries are defined as acute, subacute, and chronic with acute injuries being defined as those treated within 10–14 days of the initial trauma, subacute injuries being defined as those treated within 14 days to 6  weeks of trauma, and chronic injuries being defined as those treated after 6 weeks of the original injury.

Management Considerations The Leddy-Packer classification is very important for both directing the options for management and the ideal timeframe in which these injuries should be managed. Type I injuries are the most concerning avulsion injuries, and early referral is warranted to facilitate timely treatment, ideally within the first week of injury. As a result of the disruption of both vincula, the vascularity of the tendon is severely compromised. Without the tethering effect of the intact vincula, the tendon is able to retract to the level of the palm. As such, the goal of early management of Type I injuries is to prevent

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Figure 2.2  Clinical appearance of FDP avulsion injury in the same patient. Note the loss of normal cascade with the small finger sitting in an extended position

tendon degeneration and myostatic contracture within the forearm that will prevent full range of motion. In addition, hematoma formation within the flexor sheath leads to scarring and collapse of the pulley system over time. These factors, if not addressed in a timely fashion, will contribute to tendon adhesions and reduce tendon gliding following primary repair. If ignored or left too long, a Type I injury may require a two-stage procedure to reconstruct a scarred flexor tendon sheath and permanently retracted tendon. In Type II injuries, the profundus tendon will only retract to the PIP joint as a result of the tethering effect of the intact VPL (Fig. 2.3a). The intact VPL also maintains partial blood supply to the distal tendon stump. As such Type II injuries have a greater window within which primary surgical repair is recommended and primary repair is recommended up to 6 weeks after the injury [4]; however, we would recommend earlier repair to prevent the risk of late vincula disruption and subsequent conversion to a Type I injury [18]. Similar to Type II injuries, Type III injuries, due to their attached bony fragment, maintain tendon length and preserve vincular attachments that can be repaired up to 6  weeks following injury [3]. Type IV and V injuries should be managed acutely if the tendon has retracted into or proximal to the palm.

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a

Figure 2.3  (a) Lateral radiographs of a Leddy-Packer Type II FDP avulsion injury in a rugby player in the dominant small finger. The arrow demonstrates a small bone fragment attached to the avulsed tendon. (b) Lateral radiographs of a Leddy-Packer Type V FDP avulsion injury in an American football player. The tendon is held at the A4 pulley by the avulsed bone fragment (blue arrow). There is associated fracture of the distal phalanx that is not attached to FDP (red arrow)

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b

Figure 2.3  (continued)

 reatment Principles of Acute FDP T Avulsion Injuries Type I and II injuries are managed in a similar fashion with the exception of the dissection of the proximal tendon stump. The proximal stump can be identified through a Bruner incision (Fig. 2.4a) [20]. Type I injuries will require a palmar incision to identify the proximal stump, usually at the level of the lumbrical insertion. It is important to determine the extent of proximal retraction preoperatively to facilitate surgical planning. We have found ultrasound to be the most cost-effective mechanism for identification of the proximal stump. The pulleys will usually require dilation in order to facilitate passage of the ruptured tendon distally to the distal phalanx. The FDP must pass through Camper’s chiasm. Windows within the A3 and remaining A5 pulley can facilitate tendon passage. A small pediatric feeding tube or tendon passer aids in passing the profundus tendon to the level of the DIP joint (Fig. 2.4b). Once the tendon has been passed to the level of the DIP joint, the profundus tendon must be secured back to the distal phalanx. Traditionally, the proximal end of the tendon has

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been secured with a core suture (e.g., Kessler or Bunnell) with the suture ends passed through the distal phalanx and tied over a button on the dorsum of the distal phalanx (Fig.  2.4c). The sutures may be passed through the bone by attaching them to a Keith needle which is driven through the distal phalanx on a K-wire driver. Alternatively, the tendon can be affixed to the distal phalanx using suture anchors or a combination of button-anchor techniques (Fig. 2.4d–f). A retrospective study of 26 patients after either a pullout technique or suture anchors for affixing the FDP to the distal phalanx has not demonstrated any difference in clinical outcomes between the two types of ­ repairs, but patients tend to tolerate the microsuture anchors better and return to work earlier [21]. The surgical reconstruction should be able to tolerate functional loads to permit early postoperative mobilization [3]. Type III–V injuries are treated by open reduction and internal fixation of the avulsed fracture fragment and associated distal phalanx fracture in Type V (Fig. 2.5a–d). Fixation can be achieved with K-wire, interosseous [22], or mini screw fixation [23]. If the fragment is sufficiently large in a Type III injury, the use of mini fragment plate fixation has been described [24]. If the fragment is not adequate for fixation, the tendon should be reattached directly to the distal phalanx as with a Type I or II injury. Type IV injuries should first undergo open reduction and internal fixation of the fracture with tendon insertion into the bone.

Treatment of Subacute and Chronic Injuries In the subacute timeframe, it may be possible to perform a primary tendon repair if there has not been excessive myostatic contracture and if the flexor sheath is still patent. In order to determine if primary repair is possible, a period of traction on the ruptured tendon will likely be necessary intra-

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a

b

Figure 2.4  (a) The tendon is tethered at the level of the PIPJ by the intact vincula. Through a Bruner incision, the tendon can be retrieved at level of A3 pulley. (b) The avulsed tendon has a small fragment of bone which can aid in suture fixation. (c) Pullout suture with tie-over button for FDP reinsertion into the distal phalanx (Taken from Berger and Weiss [19]). (d) Insertion of the avulsed FDP with suture anchors (Taken from Berger and Weiss [19]). (e) Diagram of insertion of avulsed FDP with combination of suture anchors and tie-over button (Taken from J Am Acad Orthop Surg 2011;19:152–162). (f) Postoperative lateral radiographs of the same patient. A suture anchor (blue arrow) combined with a tie-over button (red arrow) is used for repair

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c

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Figure 2.4  (continued)

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Figure 2.4  (continued)

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operatively to return the tendon to adequate length to repair without causing excessive PIP and DIP flexion postoperatively. If the tendon can be passed through the flexor sheath and does not cause >1  cm shortening, a primary repair is appropriate [3]. If primary repair will not be possible, treatment options should be discussed with the patient, and definitive management plans should be made based on patient and surgeon preferences and the likelihood of patient compliance with postoperative therapy protocols, particularly if FDP tendon reconstruction is planned. Other key considerations include patient symptoms (e.g., pain), the stability of the DIP joint, and the range of motion of the DIP joint. Treatment options after a delay in diagnosis include no intervention, DIP joint arthrodesis, or reconstruction of the FDP tendon. Reconstruction of the FDP tendon can be either a one- or two-stage procedure. One-stage FDP reconstruction involves primary tendon grafting and is indicated if the flexor sheath is patent, but myostatic contracture is too great for primary repair. A two-stage reconstruction is indicated if there is both myostatic contraction and excessive scarring in the flexor sheath. The flexor pulleys are reconstructed, and a Silastic rod is placed in the first stage, followed

Figure 2.5  (a) This is a Type V injury corresponding to the radiograph in Fig.  2.3b. Intraoperative photos demonstrating a limited Bruner incision to expose tendon at level of A4 pulley where it is held by the attached bony fragment. The tendon and bony fragment are passed back through a portion of A5 pulley (red arrow). (b) A longitudinal K-wire is used to temporarily immobilize the DIP joint to allow for distal phalanx fracture healing. (c) The avulsed tendon and fragment are affixed to the distal phalanx with a tie-over button. The comminution of the distal phalanx would not likely withstand bone anchor placement due to the comminution of the bone. (d) Lateral radiograph at 12 months demonstrating preservation of joint space and remodeling at site of tendon attachment (red arrow)

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by tendon grafting for FDP reconstruction in the second stage (usually 6 to 12 weeks later). FDP reconstruction is more common in subacute cases and should only be undertaken in a select group of patients that require DIP flexion (e.g., patients 30°), then it is considered unstable, and surgical fixation is warranted [8]. The Russe classification developed in 1960, is based on fracture orientation and separates scaphoid fractures into transverse, vertical oblique and horizontal patterns. The transverse pattern is the most common type and is seen in approximately 60% of scaphoid fractures. The horizontal oblique pattern occurs in approximately 35% of scaphoid fractures and is considered to be less stable than simple transverse fractures. The vertical oblique pattern occurs in only 5% of scaphoid fractures but is considered to be the most unstable of the three patterns and typically requires operative management [33]. The modified Hebert classification system is based on a combination of fracture stability and timing of injury [21, 30, 32]. Type A fractures represent acute, stable fractures; Type B fractures represent acute, unstable fractures; Type C fractures represent delayed unions; and Type D fractures represent nonunions. Each group is then further subdivided based on different patterns of injury and displacement. Type A fractures are divided into tubercle fractures (A1) and incomplete fractures of the scaphoid waist (A2). Type B fractures are separated into oblique fractures of the distal third (B1), complete fractures of the scaphoid waist (B2), proximal pole fractures (B3), fracture dislocations (B4) and comminuted fractures (B5). In this modified system, B3 fractures are further divided into B3a and B3b based on a scapholunate angle less than or greater than 60 degrees, respectively [3]. Type C fractures represent all fractures with delayed healing of greater than 4 months. Finally, Type D fractures are subdivided based on the presence of a fibrous (D1) or sclerotic (D2) nonunion. These can be further divided based on the degree of shortening and evidence of degenerative changes (scaphoid nonunion advanced collapse).

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Treatment Closed Treatment of Scaphoid Fractures Patient-specific factors play an important role in determining treatment and are as equally important as location, displacement and fracture orientation. Socioeconomic and psychiatric factors also play a significant role in the treatment of all scaphoid fractures, but in athletes these factors are even more important [32]. Immobilisation is associated with stiffness, weakness and deconditioning, which may cause significant impairment in the competitive athlete [3]. However, this form of treatment may be acceptable for some athletes depending on the demands of their position. There is controversy regarding the treatment of non-­ displaced or minimally displaced scaphoid fractures. Choosing the optimal treatment in the competitive athlete adds a further level of complexity. Non-displaced distal pole fractures can be treated with cast immobilisation for 6  weeks with excellent healing rates [3]. Studies have shown fracture healing rates with casting to be between 87% and 95% for non-­ displaced scaphoid waist fractures [3, 9, 32]. Grewal et al. [19] showed equivalent union rates in a large series of scaphoid fractures treated non-operatively, regardless of fracture location. They did, however, see longer times to healing with more proximal fractures. When non-operative treatment is chosen, controversy exists regarding specific aspects of immobilisation including wrist position, adjacent joint incorporation and duration of casting. With regard to wrist position, considerable variation exists. Some advocate immobilising the wrist in flexion, while others recommend immobilisation in hyperextension [20]. Still, others advocate placement of the wrist in flexion and radial deviation to relax the radioscaphocapitate ligament and achieve higher union rates [8]. Despite these variations, there have been no clinical data supporting better union rates with one particular position [20]. However, evidence does show that immobilisation in 20° flexion leads to greater

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restriction of wrist extension 3 months after discontinuation of immobilisation [20]. Typically, immobilisation with the wrist in neutral to slight extension is recommended. The use of long-arm versus short-arm casts for scaphoid fractures continues to be the subject of debate. Initially, the protocol for closed treatment involved 4 weeks of long-arm casting followed by short-arm casting until fracture healing. In 1989, Gellman et al. performed a prospective, randomised controlled trial on cast immobilisation of 51 acute, non-­ displaced scaphoid fractures with this protocol. Although the study found the union rates between long- and short-arm casting to be similar, long-arm casting allowed for faster healing (9.5 weeks compared with 12.7 weeks) [17]. A more recent meta-analysis showed no significant evidence to support superiority of long-arm casting over short-arm casting [42]. As a result, exclusive short-arm casting has become much more prevalent. In athletes, the decision on long-arm or short-arm casting is still variable, but typically short-arm casting is utilised. Long-arm casting may be considered if the patient has continued pain with an initial trial of short-arm casting or in patients where non-compliance is a concern. Immobilisation of the thumb is also controversial. Conventional wisdom has held that the thumb should be held in a position of opposition to reduce the distracting forces of the abductor pollicis longus and brevis. Clay et  al. [7] performed a prospective, randomised, controlled trial and found no difference with regard to union rates with thumb-spica casting and thumb-free casting at 6 months. Despite the findings of this study, thumb-spica casting still appears to be the norm for non-operative treatment of athletes with scaphoid fractures [3, 32]. Duration of immobilisation plays an important role in determining if conservative treatment is an option. This is based on the location and stability of the fracture as outlined in the classification section of this chapter. The typical teaching is that tuberosity fractures can heal within 6 weeks, non-­ displaced distal-third fractures and waist fractures may take up to 10–12 weeks and non-displaced proximal-third ­fractures

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may take up to 4–6 months to fully heal. As mentioned earlier, with prolonged immobilisation, the risks of disuse osteopenia, deconditioning and stiffness greatly increase and may not be an option for the competitive athlete [3, 35]. Regardless of the location, all fractures treated with immobilisation require frequent office visits with serial radiographs. Evidence of displacement, collapse or cystic resorption necessitates conversion to operative treatment.

Surgical Treatment of Scaphoid Fractures Scaphoid fractures with displacement, angulation or comminution are best treated with operative intervention. Choosing the best treatment is riskier in an athlete with a non-displaced scaphoid fracture. Closed treatment carries 87–95% union rates but may require 10–12 weeks of immobilisation [3, 9, 32]. In fractures of the proximal pole, union rates are much lower (65%) and also require significantly more time (4–6 months) [8]. Percutaneous screw fixation of non-­ displaced scaphoid waist fractures offers significant benefits over closed treatment in the competitive athlete including earlier time to mobilisation, faster healing, improved motion and earlier return to work/play. A prospective, randomised controlled study by Bond et al. [4] on acute, non-displaced scaphoid waist fractures showed faster time to union (7 versus 12  weeks) and faster return to work (8 versus 15 weeks) in military personnel treated with percutaneous screw fixation compared with cast immobilisation. However, 2 years after surgery, they did not find a difference with regard to range of motion, grip strength or patient satisfaction. A more recent prospective, randomised controlled trial found range of motion, patient satisfaction and grip strength to be significantly better in the group managed operatively up to 8 weeks post-operatively [9]. Grip strength remained better in the operative group at 3 months, but after this time point, no significant difference was detected between the two groups with respect to these outcome

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measures. They also found that 10 of the 44 fractures treated non-operatively had not healed radiographically by 12 weeks, while all fractures in the operative group had healed. From these data, they recommended earlier conversion to operative fixation if there was no evidence of healing by 6–8 weeks. Despite these promising results, percutaneous fixation is not without risks. Infection and hypertrophic scar formation has been encountered with percutaneous fixation [9]. Union rates are not 100%, and the procedure can be associated with all of the expected complications associated with reduction and fixation of any fracture [6]. Percutaneous screw fixation has also been favoured over traditional open approaches in minimally displaced scaphoid fractures that are easily reduced. Although the traditional open approach allows for better visualisation of fracture reduction and more accurate fixation, it comes at the cost of increased dissection, which may disrupt the vascularity and important volar radial carpal or dorsal capsular ligaments. Studies have shown excellent results in the treatment of minimally displaced scaphoid fractures treated with percutaneous fixation [4, 34]. Open reduction and internal fixation are typically recommended for displaced fractures of greater than 1–2 mm, significant comminution, unstable fracture patterns and proximal pole fractures [32]. Fractures with concomitant carpal instability, such as a trans-scaphoid perilunate dislocation or scapholunate interosseous ligament (SLIL) injury, should be treated with open reduction and internal fixation. Open reduction and fixation is also used in cases of scaphoid nonunion when there is associated deformity of the scaphoid, such as humpback posture. A volar approach is typically used for displaced distal-third fractures, while a dorsal approach is used for displaced proximal-third fractures. Scaphoid waist fractures can be treated via either approach, with decision typically based on surgeon preference. The volar approach has the advantages of better visualisation of the distal aspect of the scaphoid, less injury to the vascular supply and improved ability to correct scaphoid

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deformity or collapse. However, failure to repair volar ligaments during the exposure can lead to secondary carpal instability [5]. Hypertrophic scarring causing pain and decreased wrist extension has also been reported [9]. The incision for this approach begins over the scaphoid tubercle. Proximal to the tubercle a longitudinal 3  cm incision is made in line with the flexor carpi radialis (FCR) tendon. Distal to the tubercle, the incision is angled towards the base of the thumb over the scaphotrapezotrapezoidal (STT) joint. The superficial palmar branch of the radial artery is identified and ligated. The FCR sheath is longitudinally incised as far distal as possible, and the FCR tendon is retracted in an ulnar direction. This will expose the floor of the FCR sheath that is confluent with the volar capsule. The capsule, including the radioscaphocapitate ligament, is divided. By elevating only the capsule that is radial to the floor of the FCR sheath, most of the volar capsule is left intact. Concomitant wrist dorsiflexion and axial traction on the thumb can aid greatly in properly exposing the distal scaphoid. A potential issue with this approach is that proper screw trajectory into the distal ulnar tip of the scaphoid can be hindered by the trapezium [24]. If this occurs, the scaphotrapezial joint must be identified and exposed. This involves a slightly deeper dissection distally and division of the origin of the thenar muscles. Once identified, the scaphotrapezial (ST) ligament is divided, and the joint capsule is opened. A small piece of the non-articulating portion of the trapezium can then be removed permitting better screw trajectory. Although there is a potential risk of scaphotrapezial arthritis with this technique, studies have not shown this to be the case [18]. Once fixation is completed, the volar capsule is repaired to restore the integrity of the radioscapholunate ligament. The dorsal approach has the advantages of better visualisation of the proximal aspect of the scaphoid and preservation of the volar ligaments and permits evaluation of the SLIL. Using the dorsal approach, it is our bias that it is easier to place the screw in a more central location. Soubeyrand et  al. [37] found that the dorsal approach allowed a more perpendicular place of a screw for an oblique fracture of the

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scaphoid waist. This approach does carry the potential risk of injury to the tenuous proximal blood supply, but multiple studies have shown no increased risk of avascular necrosis [2, 11, 28]. Regardless of whether the screw is placed through an open approach or percutaneously, the goal is adequate fracture stabilisation. Biomechanical studies have shown that rigidity of fixation is optimised with longer length screws placed down the central axis of the scaphoid [10, 26]. In order to achieve maximum screw length, screw fixation should be just below the subchondral bone. This can be difficult to judge on fluoroscopy alone and can lead to prominent screw placement [38]. Studies on percutaneous antegrade screw fixation have shown that proper placement of the screw is best performed via direct visualisation [38]. This has caused many to advocate a limited dorsal approach over straight percutaneous fixation. Also, Adamany et al. [1] found that dorsal percutaneous fixation risked injury to the posterior interosseous nerve (PIN), extensor digitorum communis (EDC) to the index finger and extensor indicis proprius (EIP). With respect to the guide wire, they found both the PIN and EDC to the index finger to be within 2.2  mm and the EIP to be within 3.1  mm. A limited volar approach is also recommended because of the typical need for partial trapezial excision in order to achieve central screw placement. Arthroscopic-assisted fixation of scaphoid fractures can also be performed to fully visualise the proper starting point for screw fixation on the proximal articular cartilage. Proponents of this technique cite the ability to evaluate and treat associated soft tissue injuries as well [14, 15]. Also, arthroscopy limits the need for wrist hyperflexion during screw insertion, preventing potential distraction of the fracture and development of humpback deformity [15]. The arthroscope is placed into the 3–4 portal, and a 6R portal is created for instrumentation. A thorough debridement of dorsal synovium adjacent to the scaphoid should be performed to allow for proper visualisation of the proximal articular surface. Once evaluation and treatment of any associated soft tissue injuries are completed, the arthroscopic camera is

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placed into the 6R portal, and the wrist is flexed to 30°. As described by Geissler [15], a 14-gauge needle is placed through the 3–4 portal and impaled into the proximal pole of the scaphoid at the insertion of the SLIL. The starting point is then verified via fluoroscopy, and the guide wire is then inserted through the needle. PA, lateral and oblique fluoroscopic images are then obtained to verify guide wire position prior to screw fixation. Excellent results have been seen with this technique, with union rates as high as 100% [15, 36]. We have chosen to approach most acute scaphoid fractures via a mini-open dorsal approach (Fig.  9.5), in some instances with arthroscopic assistance. A straight dorsal incision is made over Lister’s tubercle and extended distally for approximately 2 cm. The retinaculum between the fourth and second compartments is divided. Typically, EPL tendon is left undisturbed. The dorsal capsule is divided via a longitudinal incision from the dorsal rim of the radius and extended distally to the dorsal intercarpal ligament. Palmar flexion of the wrist allows exposure of the proximal pole of the scaphoid. The SLIL can be inspected. Reduction and temporary fixation is performed with a guide wire and if necessary a second anti-rotation pin placed down the longitudinal axis parallel to and remote from the path of the screw. Accuracy of wire placement is initially verified by fluoroscopy with the wrist flexed to ensure that the guide pin is not bent. If pin placement appears acceptable, the pins can be advanced through the volar aspect of the palm so that final confirmation can be made with the wrist extended and in slight ulnar deviation. Arthroscopy of the radiocarpal and midcarpal joints is performed if there is any question about adequacy of the reduction or intrusion of hardware into articular surface. The hand and wrist are then suspended in a traction tower. An arthroscope is inserted into the ulnar midcarpal portal. From this vantage point, the reduction of the midcarpal surface is confirmed, as is the stability of the construct. The arthroscope is then placed in the radiocarpal joint confirming the reduction of the scaphoid on its radial surface. The wrist is flexed, and the pins are advanced back through the dorsal incision. The length of the screw is confirmed.

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a

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Figure 9.5  (a) Avulsion fracture, proximal pole of scaphoid in professional baseball player. Coronal view, MR. (b) Avulsion fracture, proximal pole of scaphoid in professional baseball player sagittal view, CT. (c) Exposed proximal pole scaphoid fracture via “mini-­ open” dorsal approach. (d) De-rotation pins and screw in place. (e) Intraoperative fluoroscopic image of screw placement. (f) Axial CT image of healed scaphoid fracture at 7 weeks post-operatively

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d

Figure 9.5  (continued)

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Figure 9.5  (continued)

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Cannulated drills are inserted over the guide wire, and the screw is inserted. Wires are removed, and reduction of the scaphoid is confirmed with fluoroscopy and repeat arthroscopy of the radiocarpal and midcarpal joints.

Return to Play Determining when an athlete can return to sporting activity depends on many factors and is individualised for each patient. Fracture type, method of treatment, type of sport and player position are all factors that are taken into account. In athletes that participate in non-contact sports that do not require upper extremity use, return to play can occur immediately if cast immobilisation is planned [3, 23]. In those that undergo operative fixation, return to play is permitted when incisions are sealed and pain is controlled. Significant controversy exists in return to play in athletes that participate in contact sports or in non-contact sports where upper extremity use is required. For patients with non-­ displaced stable fractures, it is important to determine the amount of wrist motion the athlete needs in that upper extremity to return to competitive activity. If the athlete can return to play with immobilisation, a discussion with the athlete should follow regarding risk of fracture displacement and nonunion. Most of these athletes choose to return to play immediately. We have no data on healing rates in this setting. Anecdotal experience suggests that most of these fractures heal. Those that do not are treated with operative fixation at the end of the season. An athlete that requires wrist motion for his or her sport may or may not be able to compete with a fractured scaphoid. In some situations, athletes have chosen to compete with a scaphoid fracture. In these instances, the athlete is taped for competition and is casted or splinted for practice and downtime (Fig.  9.6). With this regimen, the athlete may go on to heal the fracture or will require operative treatment at the end of the season.

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b

Figure 9.6  (a) AP view of a non-displaced scaphoid waist fracture diagnosed 3 weeks after extension injury to the non-dominant wrist of a professional baseball player. The player chose to finish the season. The wrist was immobilised in a short-arm thumb-spica splint for practice and rest. For games the wrist was taped in short-arm thumb-­ spica configuration. (b) Coronal view of wrist 6 weeks after diagnosis and 9 weeks after initiating a part-time course of immobilisation to permit finishing the season as a baseball pitcher

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If the athlete cannot compete, the decision is made between operative and non-operative treatment. It is our practice to obtain serial CT scans until there is evidence of bridging bone [3, 23]. Rehabilitation follows, and the athlete is allowed to return to play when he has sufficient pain relief and grip strength equal to 80% of the contralateral hand.

Summary Scaphoid fractures are challenging to manage, and delay in diagnosis remains an issue. Once a fracture is confirmed, specific treatment plan has to be individualised taking into account the injury factors (fracture pattern, fracture location, timing of injury) and the patient factors (type of sport, position of play, timing of season). The aim of treatment would be to achieve bony union with the least amount of morbidity in order to facilitate the quickest and safest return to play for the athlete.

References 1. Adamany DC, Mikola EA, Fraser BJ.  Percutaneous fixation of the scaphoid through a dorsal approach: an anatomic study. J Hand Surg Am. 2008;33(3):327–31. 2. Bedi A, Jebson PJ, Hayden RJ, Jacobson JA, Martus JE. Internal fixation of acute, nondisplaced scaphoid waist fractures via a limited dorsal approach: an assessment of radiographic and functional outcomes. J Hand Surg Am. 2007;32(3):326–33. 3. Belsky MR, Leibman MI, Ruchelsman DE. Scaphoid fracture in the elite athlete. Hand Clin. 2012;28(3):269–78. 4. Bond CD, Shin AY, McBride MT, Dao KD. Percutaneous screw fixation or cast immobilization for non-displaced scaphoid fractures. J Bone Joint Surg Am. 2001;83-A(4):483–8. 5. Buijze GA, Lozano-Calderon SA, Strackee SD, Blankevoort L, Jupiter JB. Osseous and ligamentous scaphoid anatomy: part I. A systematic literature review highlighting controversies. J Hand Surg Am. 2011;36(12):1926–35.

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6. Bushnell BD, McWilliams AD, Messer TM.  Complications in dorsal percutaneous cannulated screw fixation of nondisplaced scaphoid waist fractures. J Hand Surg Am. 2007;32(6):827–33. 7. Clay NR, Dias JJ, Costigan PS, Gregg PJ, Barton NJ.  Need the thumb be immobilised in scaphoid fractures? A randomized prospective trial. J Bone Joint Surg Br. 1991;73(5):828–32. 8. Cooney WP, Dobyns JH, Linscheid RL. Fractures of the scaphoid: a rational approach to management. Clin Orthop. 1980;149: 90–7. 9. Dias JJ, Dhukaram V, Abhinav A, Bhowal B, Wildin CJ. Clinical and radiological outcome of cast immobilization versus surgical treatment of acute scaphoid fractures at a mean follow-up of 93 months. J Bone Joint Surg Br. 2008;90(7):899–905. 10. Dodds SD, Panjabi MM, Slade JF 3rd. Screw fixation of scaphoid fractures: a biomechanical assessment of screw length and screw augmentation. J Hand Surg Am. 2006;31(3):405–13. 11. dos Reis FB, Koeberle G, Leite NM, et  al. Internal fixation of scaphoid injuries using the Herbert screw through a dorsal approach. J Hand Surg Am. 1993;18:792–7. 12. Duckworth AD, Jenkins PJ, Aitken SA, Clement ND, Court-­ Brown CM, McQueen MM.  Scaphoid fracture epidemiology. J Trauma Acute Care Surg. 2012;72:E41–5. 13. Eastley N, Singh H, Dias JJ, Taub N. Union rates after proximal scaphoid fractures; a meta-analyses and review of available evidence. J Hand Surg Eur. 2013;38(8):888–97. 14. Geissler WB. Carpal fractures in athletes. Clin Sports Med. 2001 Jan;20(1):167–88. 15. Geissler WB. Arthroscopic management of scaphoid fractures in athletes. Hand Clin. 2009 Aug;25(3):359–69. 16. Gelberman RH, Menon J. The vascularity of the scaphoid bone. J Hand Surg Am. 1980;5:508–13. 17. Gellman H, Caputo RJ, Carter V, Aboulafia A, McKay M.  Comparison of short and long thumb-spica casts for non-­ displaced fractures of the carpal scaphoid. J Bone Joint Surg Am. 1989;71-A:354–7. 18. Geurts G, van Riet R, Meermans G, Verstreken F. Incidence of scaphotrapezial arthritis following volar percutaneous fixation of nondisplaced scaphoid waist fractures using a transtrapezial approach. J Hand Surg Am. 2011;36(11):1753–8. 19. Grewal R, Suh N, Macdermid JC. Use of computed tomography to predict union and time to union in acute scaphoid fractures treated nonoperatively. J Hand Surg Am. 2013;38(5):872–7.

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20. Hambidge JE, Desai VV, Schranz PJ, Compson JP, Davis TR, Barton NJ.  Acute fractures of the scaphoid. Treatment by cast immobilization with the wrist in flexion or extension. J Bone Joint Surg Br. 1999;81(1):91–2. 21. Herbert TJ, Fisher WE. Management of the fractured scaphoid using a new bone screw. J Bone Joint Surg Br. 1984;66-B:114–23. 22. Jonsson BY, Siggeirsdottir K, Mogensen B, Sigvaldason H, Sigursson G. Fracture rate in a population-based sample of men in Reykjavik. Acta Orthop Scand. 2004;75:195–200. 23. Kovacic J, Bergfeld J.  Return to play issues in upper extremity injuries. Clin J Sport Med. 2005;15(6):448–52. 24. Levitz S, Ring D. Retrograde (volar) scaphoid screw insertion-a quantitative computed tomographic analysis. J Hand Surg Am. 2005;30(3):543–8. 25. Majima M, Horii E, Matsuki H, Hirata H, Genda E. Load transmission through the wrist in the extended position. J Hand Surg Am. 2008;33:182–8. 26. McCallister WV, Knight J, Kaliappan R, Trumble TE.  Central placement of the screw in simulated fractures of the scaphoid waist: a biomechanical study. J Bone Joint Surg Am. 2003;85-A(1):72–7. 27. Parvizi J, Wayman J, Kelly P, Moran CG. Combining the clinical signs improves diagnosis of scaphoid fractures: a prospective study with follow-up. J Hand Surg Br. 1998;23:324–7. 28. Rettig ME, Raskin KB. Retrograde compression screw fixation of acute proximal pole scaphoid fractures. J Hand Surg Am. 1999;24:1206–10. 29. Riester JN, Baker BE, Mosher JF, Lowe D. A review of scaphoid fracture healing in competitive athletes. Am J Sports Med. 1985;13(3):159–62. 30. Ring D, Jupiter JB, Herndon JH. Acute fractures of the scaphoid. J Am Acad Orthop Surg. 2000;8:225–31. 31. Ring D, Lozano-Calderón S.  Imaging for suspected scaphoid fracture. J Hand Surg Am. 2008;33:954–7. 32. Rizzo M, Shin AY. Treatment of acute scaphoid fractures in the athlete. Curr Sports Med Rep. 2006;5(5):242–8. 33. Russe O.  Fracture of the carpal navicular: diagnosis, non-­ operative treatment, and operative treatment. J Bone Joint Surg Am. 1960;42:759–68. 34. Saeden B, Tornkvist H, Ponzer S, Hoglund M.  Fracture of the carpal scaphoid: a prospective, randomized 12-year follow-up comparing operative and conservative treatment. J Bone Joint Surg Br. 2001;83(2):230–4.

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35. Skirven T, Trope J. Complications of immobilization. Hand Clin. 1994;10(1):53–61. 36. Slade JF 3rd, Gutow AP, Geissler WB. Percutaneous internal fixation of scaphoid fractures via an arthroscopically assisted dorsal approach. J Bone Joint Surg Am. 2002;84-A(Suppl 2):21–36. 37. Soubeyrand M, Biau D, Mansour C, Mahjoub S, Molina V, Gagey O.  Comparison of percutaneous dorsal versus volar fixation of scaphoid waist fractures using a computer model in cadavers. J Hand Surg Am. 2009;34(10):1838–44. 38. Tumilty JA, Squire DS. Unrecognized chondral penetration by a Herbert screw in the scaphoid. J Hand Surg Am. 1996;21(1):66–8. 39. Unay K, Gokcen B, Ozkan K, Poyanli O, Eceviz E. Examination tests predictive of bone injury in patients with clinically suspected occult scaphoid fracture. Injury. 2009;40:1265–8. 40. Van Tassel DC, Owens BD, Wolf JM.  Incidence estimates and demographics of scaphoid fracture in the US population. J Hand Surg Am. 2010;35A:1242–5. 41. Wolf JM, Dawson L, Mountcastle SB, Owens BD.  The incidence of scaphoid fracture in a military population. Injury. 2009;40:1316–9. 42. Yin ZG, Zhang JB, Kan SL, Wang P. Treatment of acute scaphoid fractures: systematic review and meta-analysis. Clin Orthop Relat Res. 2007 Jul;460:142–51. 43. Yin ZG, Zhang JB, Kan SL, Wang XG.  Diagnosing suspected scaphoid fractures: a systematic review and meta-analysis. Clin Orthop Relat Res. 2010;468:723–34. 44. Yin ZG, Zhang JB, Kan SL, Wang XG.  Diagnostic accuracy of imaging modalities for suspected scaphoid fractures: meta-­ analysis combined with latent class analysis. J Bone Joint Surg Br. 2012;94-B(8):1077–85.

Chapter 10 Carpal Fractures (Excluding Scaphoid) Carlos Heras-Palou

Key Learning Points Recognise injuries to the carpal bones, and appreciate that some can be managed non-operatively, whilst others require early operative intervention in the athlete.

Introduction Two thirds of carpal fractures involve the scaphoid. The other bones in the carpus are involved less frequently, in the order triquetrum (15%), trapezium (6%), pisiform (4%), capitate (2%), hamate (2%), lunate (1%) and trapezoid ( 20 mmHg [2]. More recently, authors have also suggested any P > 30 mmHg during exercise [3] or a rise of 10 mmHg with exertion regardless of baseline [9]. Dynamic compartment pressure monitoring is carried out under local anaesthetic. Pressures can be measured in the superficial flexor compartment and both extensor compartments, but not the deep flexor compartment due to the risk of neurovascular injury. Purpose-built needle pressure transducers can be used (Fig.  14.2  – Stryker Intracompartmental Pressure Monitor, Stryker Corp) but require to be introduced repeatedly for serial measurements pre- and postexercise. The author prefers a technique where cannulae are sited for the duration of the study. The tip of a large bore (18G) Venflon is sited in the desired muscle compartment, and the Venflon is taped to the skin. The Venflon is connected to an arterial line pressure transducer on an anaesthetic trolley to give a constant trace. It should be noted that the pressure transducer has to be at the same height as the needle tip, or a false reading will be given. Intracompartmental pressures are

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measured at rest and at the onset of symptoms when the patient has exercised (a simple grip strengthening device is generally used). Further readings are taken at 1- and 5-min post-onset of symptoms.

Treatment This involves avoidance of the precipitating activity. However, in elite and professional athletes, this will not be acceptable. Treatments such as physiotherapy including deep massage and stretches, as well as a review of technique, such as with rowers and kayakers, have generally already been tried before referral to a surgeon. The gold standard remains four-­ compartment fasciotomy with good to excellent results reported in 80–90% of patients [10]. Fasciectomy has been described but requires a longer recovery period and has not shown improved results over a simple fasciotomy [20]. The incidence of complications is low and includes haematoma, neurovascular injury, muscle hernia and continuing or recurrent symptoms. In acute compartment syndrome, a fasciotomy requires full-length skin incisions due to the often gross swelling of the limb and resulting skin tightness (Fig. 14.3). In the treatment of CECS, more minimal skin incisions are used [7] (Fig. 14.4). Studies have suggested that leaving skin ‘bridges’ results in higher intracompartmental pressures than if a full-length dermotomy has been performed, but this does not seem to be clinically relevant in CECS [8]. Various anatomical approaches have been suggested to allow adequate decompression of the affected muscle compartments. For the flexor compartment, an internervous approach between FCU (ulnar nerve) and FDS (median nerve) releases the fascia over the superficial compartment and the biceps aponeurosis and allows access to the deep flexor compartment [14]. In trauma, a Henry’s approach is

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Figure 14.3 Scar from volar fasciotomy for acute compartment syndrome in a child

the most common approach to the volar aspect of the forearm as it allows safe access to the radius for fracture fixation. However, it is noted that a Henry’s approach requires release of the pronator teres tendon off the radius to adequately decompress the deep flexor compartment, and therefore, in CECS this may lead to a delay in recovery and possibly even functional loss. Minimally invasive techniques have been described with excellent results reported and early return to full function [5]. A specialist endoscopic knife is used to release both extensor and the superficial flexor muscle compartments and a standard knife to release the deep flexor compartment. Several 2  cm incisions are made with no complications reported in eight patients. More recently, endoscopic techniques have been used that allow less scarring and possibly a faster return to full function [13, 17]. Release of both

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Figure 14.4  Minimal skin incisions for fasciotomy in the treatment of CECS

the flexor and extensor compartments has been described using endoscopic techniques. It is noted that a release of the deep flexor compartment is not performed with these techniques. This would tend to support studies that suggest release of the fascia over the superficial flexor compartment alone will adequately decompress both superficial and deep compartments [4]. Recovery is rapid once the skin incisions have healed with a return to training at 2–3 weeks. A suggested timetable for recovery is given (Table 14.1). Studies suggest a return to full training and actual competition by 6 weeks.

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Table 14.1  Forearm fasciotomy – guideline for recovery Day Activities 0–14 Rest arm in a sling Very gentle hand, wrist and elbow range of movement exercises 4 x daily Avoid gripping – can do gentle, everyday activities, e.g. holding spoon/cup Reduce pressure dressing at day 7 Keep skin dressings in place No formal aerobic activity 14–28

Skin dressings removed at day 14 Physiotherapy to help reduce scar tethering and regain full arm movements Begin aerobic training using static bike and running modalities Start exercising the arms – gym/rowing machine

28–42+

Aim to graduate back to full training Look to build volume and intensity gradually

Summary Chronic exertional compartment syndrome (CECS) of the forearm is a common and disabling condition that affects athletes that are required to perform repetitive contractions of the forearm musculature. Transient symptoms often settle with a period of rest, but more permanent symptoms often require surgical decompression which is successful in the majority of cases. The diagnosis is often clinical based mainly on the history, but compartment pressure measurements may help in equivocal cases.

Questions and Answers Questions 1. A body builder wakes at night with numbness affecting his little finger. He has noted he is struggling to lift heavier

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weights and feels his grip strength is less. How would you manage this patient? 2. A professional motorcyclist has signed for a team using 1000 cc bikes. He has noticed he is struggling to control the bike in the second half of races. Clinical examination is normal. How do you proceed?

Answers 1. This is likely to be a peripheral nerve problem. I would take a full history asking about any precipitating factors including any numbness when exercising, any trauma to his elbow (the usual site of compression of the ulnar nerve), and does he have diabetes. I would examine him looking for any fixed flexion deformity in his elbow, does he have a positive Tinel’s test at the cubital tunnel at his elbow, muscle wasting in his hand and check for numbness in an ulnar nerve distribution. Finally, I would organise nerve conduction studies to confirm the diagnosis. 2. The increase to larger engine bikes significantly increases the loading through the forearm when gripping. I would take a detailed history asking how long he has been affected, whether both arms are affected, does he have any finger numbness at any time, does he get locking out of the forearm muscles, do symptoms affect him at any other time, and are both the flexor and extensor compartments affected. I would explain the likely diagnosis of exercise induced compartment syndrome, encourage him to try all treatment modalities such as relaxation techniques while riding, and physiotherapy working on massage and stretching exercises. If his symptoms persist it is likely surgery will be indicated.

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References 1. Allen MJ, Barnes MR.  Chronic compartment syndrome of the flexor muscles in the forearm: a case report. J Hand Surg Br. 1989;14(1):47–8. 2. Amendola A, Rorabeck CH, Vellett D, et al. The use of magnetic resonance imaging in exertional compartment syndromes. Am J Sports Med. 1990;18(1):29–34. 3. Brown JS, Wheeler PC, Boyd KT, Barnes MR, Allen MJ. Chronic exertional compartment syndrome of the forearm: a case series of 12 patients treated with fasciotomy. J Hand Surg Eur Vol. 2011;36(5):413–9. 4. Chan PS, Steinberg DR, Pepe MD, Beredjiklian PK.  The significance of the three volar spaces in forearm compartment syndrome: a clinical and cadaveric correlation. J Hand Surg Am. 1998;23(6):1077–81. 5. Croutzet P, Chassat R, Masmejean EH. Mini-invasive surgery for chronic exertional compartment syndrome of the forearm: a new technique. Tech Hand Up Extrem Surg. 2009;13(3):137–40. 6. Detmer DE, Sharpe K, Sufit RL, Girdley FM. Chronic compartment syndrome: diagnosis, management, and outcomes. Am J Sports Med. 1985;13(3):162–70. 7. Harrison JW, Thomas P, Aster A, Wilkes G, Hayton MJ. Chronic exertional compartment syndrome of the forearm in elite rowers: a technique for mini-open fasciotomy and a report of six cases. Hand (N Y). 2013;8(4):450–3. 8. Havig MT, Leversedge FJ, Seiler JG.  Forearm compartment pressures: an in  vitro analysis of open and endoscopic assisted fasciotomy. J Hand Surg Am. 1999;24(6):1289–97. 9. Hutchinson M. Chronic exertional compartment syndrome head to head. Br J Sports Med. 2011;45:954–5. 10. Jans C, Peersman G, Peersman B, Van Den Langenbergh T, Valk J, Richart T.  Endoscopic decompression for chronic compartment syndrome of the forearm in motocross racers. Knee Surg Sports Traumatol Arthrosc. 2014. (Epub ahead of print). 11. Mavor GE. The anterior tibial syndrome. JBJS. 1956;38-B:513–7.

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12. Pedowitz RA, Hargens AR, Mubarak SJ, Gershuni DH. Modified criteria for the objective diagnosis of chronic compartment syndrome of the leg. Am J Sports Med. 1990;18(1):35–40. 13. Pozzi A, Pivato G, Kask K, Susini F, Pegoli L. Single portal endoscopic treatment for chronic exertional compartment syndrome of the forearm. Tech Hand Up Extrem Surg. 2014;18(3):153–6. 14. Ronel DN, Mtui E, Nolan WB. Forearm compartment syndrome: anatomical analysis of surgical approaches to the deep space. Plast Reconstr Surg. 2004;114(3):697–705. 15. Rorabeck CH, Macnab I.  The pathophysiology of the ante rior tibial compartmental syndrome. Clin Orthop Relat Res. 1975;113:52–7. 16. Rydholm U, Werner CO, Ohlin P.  Intracompartmental fore arm pressure during rest and exercise. Clin Orthop Relat Res. 1983;(175):213–5. 17. Seiler JG 3rd, Hammond KE, Payne SH, Ivy R. Bilateral exertional compartment syndrome of the forearm: evaluation and endoscopic treatment in an elite swimmer. J Surg Orthop Adv. 2011;20(2):126–31. 18. Söderberg TA. Bilateral chronic compartment syndrome in the forearm and the hand. J Bone Joint Surg Br. 1996;78(5):780–2. 19. Willick SE, Deluigi AJ, Taskaynatan M, Petron DJ, Coleman D.  Bilateral chronic exertional compartment syndrome of the forearm: a case report and review of the literature. Curr Sports Med Rep. 2013;12(3):170–4. 20. Winkes MB, Luiten EJ, van Zoest WJ, Sala HA, Hoogeveen AR, Scheltinga MR.  Long-term results of surgical decompression of chronic exertional compartment syndrome of the forearm in motocross racers. Am J Sports Med. 2012;40(2):452–8. 21. Zandi H, Bell S.  Results of compartment decompression in chronic forearm compartment syndrome: six case presentations. Br J Sports Med. 2005;39(9):e35.

Index

A A2 pulley rupture, see Climber’s pulley injuries Abductor pollicis longus (APB/ APL), 204, 228 Acute compartment syndrome (ACS), 277 Avulsions, 135 B Bennett’s fracture, 126, 129, 131 Boutonniere deformity, 40 Bow-stringing phenomenon, 90 Boxer’s fractures, 108 Boxer’s knuckle anatomy, 152, 153 clinical features, 153 investigations, 153 operative management, 153, 154 outcomes, 154 pathology, 152, 153 Buddy strapping, 65 Buddy taping, 47 Button-anchor techniques, 24

C Carpal fractures capitate fractures, 190, 191, 193 hamate fractures, 190, 192, 195–197, 200 incidence, 185, 186 lunate fractures, 197, 198 pisiform, 188, 190 trapezium, 188, 189 trapezoid, 198, 199 triquetrum, 187, 188, 200 Carpal instability complex (CIC), 213, 215 Carpal instability dissociative (CID), 213, 215 Carpal instability non-­ dissociative (CIND), 213, 215 Carpometacarpal (CMC) joint, 197 anatomy, 154, 155 clinical features, 156 operative management, 156, 157 outcome, 157 pathology, 154, 155

© Springer Nature Switzerland AG 2019 M. Hayton et al. (eds.), Sports Injuries of the Hand and Wrist, In Clinical Practice, https://doi.org/10.1007/978-3-030-02134-4

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290

Index

Chronic exertional compartment syndrome (CECS) aetiology, 278, 279 clinical diagnosis, 280–282 pathophysiology, 279, 280 treatment, 282–285 Climber’s pulley injuries biomechanics, 89 crimp grip, 82, 85, 98 DIPJ, 87 flexor tendon sheath anatomy, 83, 88 French Classification, 82, 86–87 hook grip, 82, 85, 98 International Climbing and Mountaineering Federation, 83, 86–87 IPJ, 87 MCPJ, 83 palmar aponeurosis, 87 PIPJ, 83 pulley ruptures body movements, 91 clinical assessment and classic bowstringing, 92, 93 clinical examination, 89, 90 first-aid measures, 92 imaging examination, 90, 91 pathology, 89 repeated manoeuvre, 91 results, 97 surgical technique, 94–97 training sessions, 91 treatment, 93, 94 short climbing lexicon, 82 slope grip, 82, 85, 98 Comminuted fractures, 74 Conventional therapy, 77 D Distal interphalangeal joint (DIPJ), 2, 16, 87 Distal phalanx fractures, 71, 72

Distal radio-ulnar joint (DRUJ), 262 Dorsal blocking splint, 65 Dorsal splint, 65 Doyle’s classification, 3, 4 Dynamic compartment pressure monitoring, 281 E Eaton-Belsky technique, 66, 68 Edinburgh position splint, 65 Epibasal fractures, 133 Extensor carpi radialis longus (ECRL), 228 Extensor carpi ulnaris (ECU) tendon, 204, 245 anatomy and biomechanics, 256–259 classification, 265 clinical presentation, 260 diagnosis, 263 imaging, 263 inflammatory tendinopathy, 263, 264 mechanism, 259–261 physical examination, 260, 262 RTP, 273–275 tendon protocol, 267–270, 273 tendon rupture, 263–265 traumatic instability, 263, 264 treatment decisions, 265–267 wrist taping, 268, 269 Extra-articular fractures, 133 Extra-articular metacarpal shaft fractures, 129 F Flexor carpi radialis (FCR) muscles, 228 Flexor carpi ulnaris (FCU), 203, 247 Flexor digitorum profundus (FDP) avulsion injuries anatomy, 16, 18 classification, 18, 19

Index diagnosis magnetic resonance imaging, 20 physical examination, 19 soft tissue imaging, 20 ultrasound, 20 rehabilitation programmes, 30 treatment, 20 acute principles, 23 Leddy-Packer classification, 20 management, 20, 21 mini fragment plate fixation, 24 outcomes, 31 reconstruction, 30 subacute timeframe, 24 type I and II injuries, 23 type III–V injuries, 24 G Gamekeeper’s thumb, 138 H Hebert classification system, 167 Hypertrophic scarring, 172 I Interphalangeal joint level (IPJ), 87 Intra-articular fractures, 135 Intra-compartmental pressure monitoring, 280, 281 Intrinsic plus (IPP), 65 J Jersey finger, 16 K Keith needle, 24 Kienbὅck’s disease, 197 K-wire, 24, 45

291

L Leddy-Packer classification, 20 Lister’s tubercle, 174 Lunocapitate (LC) joints, 203 Lunotriquetral (LTq) instability, 205, 206, 248 M Magnetic resonance imaging (MRI), 20, 240 Mallet injury classification, 3 clinical setting, 2 diagnosis, 3 distal phalanx, 6 treatment, 3 acute, 5 chronic lesions, 6 conservative, 4, 5, 10 mallet fracture, 7, 9 post-operative treatment, 9 pure tendinous lesion, 5 surgical treatment, 10 Mallet thumb, 135, 146 Malunion, 121 Manipulation under anaesthesia (MUA), 116 Mayo classification system, 167 Metacarpal fractures, 129 anatomy, 102–104 cascade sign, 109–111 clinical assessment, 104 immobilisation techniques, 106 metacarpal base extra-articular fractures, 118 investigation, 120 management, 120 metacarpal head investigation, 107 management, 107 referral, 107 metacarpal neck fingernail rotation, 110

292

Index

Metacarpal fractures (Cont.) investigation, 112 management, 112, 113 overlapping, 109 referral, 114 metacarpal shaft investigation, 117 management, 117 manipulation under anaesthesia, 116 non-operative, 115 referral, 117 radiographs, 105 stability, 105 treatment malunion, 121 metalwork, 121 non-union, 121 pressure effects, 121 rotational mal-alignment, 121 stiffness, 122 Metacarpophalangeal joint (MCPJ), 19, 35, 83 Metalwork, 121 Mini fragment plate fixation, 24 Minimally invasive techniques, 283 N Non-displaced distal pole fractures, 168 Non-steroidal anti-inflammatory drugs (NSAIDs), 241 O Oblique fractures, 74 P Palmar “V” Sign, 223 Phalangeal fractures, 75 assessing stability, 64, 65 clinical assessment, 62–64

middle phalanx, 72, 73 open fractures, 64 PIPJ and DIPJ, 77 proximal phalanx, 72, 73 rehabilitation, 76 return-to-play, 77 splinting buddy strapping, 65 dorsal blocking splint, 65 edinburgh position splint, 65 thimble splint, 65 volar splint, 65 surgical intervention closed reduction, 66, 69 Eaton-Belsky technique, 66–68 internal fixation, 69, 71 intramedullary wires, 67, 69 open reduction, 69, 71 percutaneous screw fixation, 69 percutaneous wiring, 66 treatment, 77 in young athletes phalangeal base fractures, 76 phalangeal neck fractures, 75 seymour fracture, 74 Phalangeal neck fractures, 75 Polydioxanone suture (PDS), 244 Posterior-anterior (PA) radiograph, 188 Pre-dynamic instabilities, 217 Proximal interphalangeal joint (PIPJ), 19, 83 anatomy, 37, 38 central slip extensor tendon injuries, 41 collateral ligament injuries, 38, 39 condylar fractures return to sport, 54 timing of surgery, 53

Index treatment, 50, 52, 53 dislocations, 38 complex dislocations, 39 dorsal fracture, 43–45 recurrent dislocations, 40 return to sport, 39 treatment, 38, 39 dorsal lip fractures, 47 palmar lip fractures, 43 phalangeal neck fractures, 55, 56 pilon fractures remodelling, 47 return to sport, 50 treatment, 49, 50 sub-condylar fractures, 55 R Return to play (RTP), 273–275 Ring’ sign, 224 Robert’s view, 131 Rolando’s fractures, 129, 132 Russe classification, 167 S Scaphocapitate (SC) joint, 203 Scaphoid fractures computed tomography, 164 diagnosis, 163, 164 Hebert classification system, 167 magnetic resonance imaging, 164 Mayo classification system, 167 proximal pole, 166 radiographs, 166 return to play, 178, 180 Russe classification, 167 snuffbox, 163 treatment arthroscopic-assisted fixation, 173 dorsal approach, 172

293

immobilisation, 169 internal fixation, 171 long-arm vs. short-arm casts, 169 mini-open dorsal approach, 174, 175 non-operative treatment, 168 open reduction, 171 percutaneous screw fixation, 171 socioeconomic and psychiatric factors, 168 straight dorsal incision, 174 volar approach, 171 Scaphoid lunate advanced collapse (SLAC), 213 Scapholunate (SL) ligament injury axial rotation, 208, 209 carpal stabilisation, 209, 210 dart-throwing motion, 206, 207, 230 distal row, 202, 203, 206 dorsal ligament, 205, 206, 230 extracapsular ligaments, 203, 204 FCU, 203 flexion-extension, 207 frontal plane of motion/ radial-ulnar inclination, 208 intracapsular ligaments, 203, 204 intrinsic ligaments, 204 kinetics, 209 midcarpal joint, 203, 206 palmar ligament, 205, 206 proprioceptive feedback, 203, 230 proximal ligament, 230 radiocarpal joint, 203 radius row, 202, 203 sagittal plane of motion, 207 SLD (see Scapholunate dissociation)

294

Index

Scapholunate dissociation (SLD), 230 arthrography, 225 arthro-MRI, 224 arthroscopy, 225 cadaveric division, 212 classification, 216, 217 degenerative changes, 213 diagnosis, 217 dynamic cineradiography, 223, 224 examination, 218–220 history, 217 loaded lunate, 212 perilunar dislocations, 210 permanent misalignment, 212 plain radiograph, 220–224 positive scaphoid shift test, 230, 231 progressive perilunar destabilisation, 211 radioscaphoid fossa, 213 stages, 213 treatment general factors, 226 local factors, 226, 227 patient selection, 226 staging, 227–229 triquetrum, 212 ultrasound, 225 wrist instability, 213, 215 Scaphotrapezotrapezoidal (STT) joint, 172, 203 Seymour fracture, 74 Skier’s thumb, 138 SL interosseous ligament (SLIL) injury, 226–229 Spiral fractures, 74 Sports injury, see Extensor carpi ulnaris (ECU) tendon Stener’s lesion, 143, 144, 146 T Terry Thomas’ sign, 222 Thimble splint, 65

Three-ligament tenodesis technique, 228, 229 Thumb metacarpal fractures Bennett’s fracture, 126, 129 extra-articular metacarpal shaft fractures, 129 head fracture, 129 imaging, 131 medical history, 129, 131 physical exam, 129, 131 Rolando fracture, 129 treatment, 131–133 Thumb phalangeal fractures avulsions, 135 extra-articular fractures, 133, 135 intra-articular fractures, 135 medical history, 143, 145 physical exam, 143, 145 radiographic evaluation, 145 treatment, 145–147 Triangular fibrocartilage complex (TFCC) acute/chronic wrist pain, 240 arthroscopic techniques, 242 biomechanical tests, 237 central articular disc, 237 cortisone injection, 241 degenerative classification, 237 degenerative tears, 241 diagnosis, 240 distal radioulnar joint, 238 distal radius, 237, 238 gripping pronation maneuver/ ulnar positive variance, 240 MRI, 240 vs. open repair, 246–250 operative intervention, 241, 242 operative setup and diagnostic arthroscopy, 242–244 repair process, 244, 245

Index resistance rotational movements, 240 specificity and sensitivity, 240 symptomatic tears, 241 traumatic classification, 236, 237 ulnar-side wrist pain, 240 vascularity, 238, 239 Triquetrocapitate (TqC) ligament, 206 Triquetrohamate (TqH) joint, 203, 206 T-shaped fracture, 47 Tuft fractures, 145

295

U Ulnar collateral ligament (UCL) injuries, 126–129 Ulnolunate (UL) ligament, 237 Ulnotriquetral (UT) ligament, 237 V Volar splint, 65 Z Zone I flexor tendon injuries, 15